Common Medical and Surgical Conditions Complicating Pregnancy

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Chapter 16 Common Medical and Surgical Conditions Complicating Pregnancy

The more common medical, infectious, and surgical disorders that may complicate pregnancy are covered in this chapter. The pharmacologic agents recommended for these disorders have been classified by the Food and Drug Administration (FDA) for fetal risk (see Box 7-1 on page 73). Up to date information on these drugs can be found at www.FDA.gov/ by selecting “Drugs” from the menu and searching for a specific agent.

image Endocrine Disorders

Diabetes mellitus and thyroid disease are the two most common endocrine disorders complicating pregnancy.

DIABETES MELLITUS

Incidence and Classification

The prevalence of diabetes mellitus has greatly increased in the last 20 years. Reports show a rate of 3% to 8% of gestational diabetes mellitus (GDM). Pregestational diabetes is present in about 1% of pregnancies. Overall, 90% of diabetes in pregnant women is gestational and about 10% pregestational.

GDM is defined as glucose intolerance with onset or first recognition during pregnancy. Pregnancy is associated with progressive insulin resistance. Human placental lactogen, progesterone, prolactin, cortisol, and tumor necrosis factor are associated with increased insulin resistance during pregnancy. Studies suggest that women who develop GDM have chronic insulin resistance and that GDM is a “stress test” for the development of diabetes in later life. Most obstetricians use White’s classification of diabetes during pregnancy. This classification is helpful is assessing disease severity and the likelihood of complications (Table 16-1).

TABLE 16-1 WHITE’S CLASSIFICATION OF DIABETES IN PREGNANCY

Class Description Therapy
A1 Gestational diabetes; glucose intolerance developing during pregnancy; fasting blood glucose and postprandial plasma glucose normal Diet alone
A2 Gestational diabetes with fasting plasma glucose >105 mg/dL; or 2-hr postprandial plasma glucose >120 mg/dL, or 1-hr postprandial plasma glucose >140 mg/dL Diet and insulin
B Overt diabetes developing after age 20 yr and duration < 10 yr Diet and insulin
C Overt diabetes developing between ages 10 and 19 yr or duration 10-19 yr Diet and insulin
D Overt diabetes developing before age 10 yr or duration 20 yr or more or background retinopathy Diet and insulin
F Overt diabetes at any age or duration with nephropathy Diet and insulin
R Overt diabetes at any age or duration with proliferative retinopathy Diet and insulin
H Overt diabetes at any age or duration with arteriosclerotic heart disease Diet and insulin

Complications

Maternal and fetal complications of diabetes are listed in Table 16-2. Diabetes often coexists with the metabolic syndrome. Most fetal and neonatal effects are attributed to the consequences of maternal hyperglycemia, or, in the more advanced classes, to maternal vascular disease. Glucose crosses the placenta easily by facilitated diffusion, causing fetal hyperglycemia, which stimulates pancreatic β cells and results in fetal hyperinsulinism. Fetal hyperglycemia during the period of embryogenesis is teratogenic. There is a direct correlation between birth defects in diabetic pregnancies and increasing glycosylated hemoglobin levels (HbA1C) in the first trimester. Fetal hyperglycemia and hyperinsulinemia cause fetal overgrowth and macrosomia, which predisposes to birth trauma, including shoulder dystocia and Erb’s’ palsy. Fetal demise is most likely due to acidosis, hypotension from osmotic dieresis, or hypoxia from increased metabolism coupled with inadequate placental oxygen transfer.

TABLE 16-2 MATERNAL AND FETAL COMPLICATIONS OF DIABETES MELLITUS

Entity Monitoring
MATERNAL COMPLICATIONS  
OBSTETRIC COMPLICATIONS  
Polyhydramnios Close prenatal surveillance; blood glucose monitoring, ultrasonography
Preeclampsia Evaluation for signs and symptoms
Infections, e.g., urinary tract infection and candidiasis Urine culture, wet mount, appropriate therapy
Cesarean delivery Blood glucose monitoring, insulin and dietary adjustment to prevent fetal overgrowth
Genital trauma Ultrasonography to detect macrosomia, cesarean delivery for macrosomia
DIABETIC EMERGENCIES  
Hypoglycemia Teach signs and symptoms; blood glucose monitoring; insulin and dietary adjustment; check for ketones, blood gases, and electrolytes if glucose > 300 mg/dL
Diabetic coma  
Ketoacidosis  
VASCULAR AND END-ORGAN INVOLVEMENT OR DETERIORATION (IN PATIENTS WITH PREGESTATIONAL DIABETES MELLITUS)
Cardiac Electrocardiogram first visit and as needed
Renal Renal function studies, first visit and as needed
Ophthalmic Funduscopic evaluation, first visit and as needed
Peripheral vascular Check for ulcers, foot sores; noninvasive Doppler studies as needed
NEUROLOGIC  
Peripheral neuropathy Neurologic and gastrointestinal consultations as needed
Gastrointestinal disturbance  
Long-Term Outcome  
Type 2 diabetes Postpartum glucose testing, lifestyle changes (diet and exercise)
Metabolic syndrome Lifestyle changes (diet and exercise)
Obesity Lifestyle changes (diet and exercise)
Cardiovascular disease Annual checkup by physician, lifestyle changes (diet and exercise)
Fetal and Neonatal Complications  
Maintenance of maternal euglycemia will decrease most of these complications.
Macrosomia with traumatic delivery (shoulder dystocia, Erb’s palsy) Ultrasonography for estimated fetal weight before delivery; consider cesarean delivery if estimated fetal weight > 4250-4500 g
DELAYED ORGAN MATURITY  
Pulmonary, hepatic, neurologic, pituitary-thyroid axis; with respiratory distress syndrome, hypocalcemia Avoid delivery before 39 weeks in the absence of maternal or fetal indications unless amniocentesis indicates lung maturity. Maintain euglycemia intrapartum.
CONGENITAL DEFECTS  
Cardiovascular anomalies Preconception counseling and glucose control, HbAlc in the first trimester
Neural tube defects Maternal serum alpha-fetoprotein screening; fetal ultrasonography and fetal echocardiogram; amniocentesis and genetic counseling
Caudal regression syndrome  
Other defects, e.g., renal  
FETAL COMPROMISE  
Intrauterine growth restriction Serial ultrasonography for fetal growth and estimated fetal weight, serial fetal surveillance with nonstress test, amniotic fluid index, and fetal Doppler. Avoid postdates pregnancy.
Intrauterine fetal death
Abnormal fetal heart rate patterns

In pregestational diabetes, maternal complications include worsening nephropathy and retinopathy, a greater incidence of preterm preeclampsia and a higher likelihood of diabetic ketoacidosis. Hypoglycemia is much more common because of the tighter control attempted during pregnancy. Fetal complications include an increased rate of abortions, anatomic birth defects, fetal growth restriction, and prematurity.

Diagnosis

Screening for gestational diabetes is generally performed between 24 and 28 weeks of gestation with a 50-g 1-hour oral glucose challenge test (GCT), given without regard to last oral intake. This timing will identify most gestational diabetic patients while providing several weeks of therapy to reduce potentially adverse consequences. Screening is advised at the first prenatal visit in pregnant women with risk factors such as maternal age greater than 25 years, previous macrosomic infant, previous unexplained fetal demise, previous pregnancy with GDM, family history of diabetes, history of polycystic ovarian disease, and obesity. If overt signs and symptoms of diabetes are present, a fetal scalp blood test should be undertaken first. If the first-trimester screen is negative, it should be repeated at 24 to 28 weeks. Glucose values above 130 to 140 mg/dL on a GCT are considered abnormal and have an 80% to 90% sensitivity in detecting GDM.

An abnormal screening GCT is followed with a diagnostic 3-hour 100-g oral glucose tolerance test. This involves checking the fasting blood glucose after an overnight fast, drinking a 100-g glucose drink, and checking glucose levels hourly for 3 hours. If there are two or more abnormal values on the 3-hour GTT, the patient is diagnosed with GDM (Table 16-3). If the 1-hour screening (50-g oral glucose) plasma glucose exceeds 200 mg/dL, a glucose tolerance test is not required and may dangerously elevate blood glucose values.

TABLE 16-3 THREE-HOUR ORAL GLUCOSE TOLERANCE TEST

Test Maximal Normal Blood Glucose (mg/dL)
Fasting 95
1 hr 180
2 hr 155
3 hr 140

From Carpenter and Coustan.

Management

Antepartum Obstetric Management

Aside from achieving euglycemia, adequate surveillance should be maintained during pregnancy to detect and possibly mitigate maternal and fetal complications. In pregestational diabetic patients, or in those with GDMs diagnosed before 20 weeks, a first-trimester dating ultrasound followed by a detailed obstetric ultrasonic study, fetal echocardiogram, and maternal serum alpha-fetoprotein level should be obtained at 16 to 20 weeks to check for congenital malformations. Maternal renal, cardiac, and ophthalmic functions must be closely monitored. The HbA1C should be obtained at the first prenatal visit, which is preferably scheduled early in the first trimester. Individuals with significantly elevated values (>8.5%) should be particularly targeted for careful ultrasonic assessment for congenital anomalies. Regular electronic, biochemical, and ultrasonographic fetal monitoring should be performed. For diabetic classes A, B, and C, fetal macrosomia is common and should be investigated, whereas for classes D, F and R, fetal growth restriction occurs more commonly.

Serial fetal testing should be performed in the third trimester. In patients with GDM on diet, fetal testing can be initiated at term; while in those on insulin, fetal testing should be initiated between 32 and 34 weeks of gestation or sooner if complications develop.

If the maternal state is stable, blood glucose is in the euglycemic range, and fetal studies indicate a healthy baby, spontaneous onset of labor at term may be awaited. Earlier intervention is indicated if these conditions are not met. For macrosomic babies, increased birth trauma to both mother and fetus should be kept in mind. Cesarean delivery may be elected for large fetuses (>4250 to 4500 g).

THYROID DISEASES

Normal Thyroid Physiology during Pregnancy

With the increase in glomerular filtration rate that occurs during pregnancy, the renal excretion of iodine increases, and plasma inorganic iodine levels are nearly halved. Goiters due to iodine deficiency are not likely if plasma inorganic iodine levels are greater than 0.08 μg/dL. Inorganic iodine supplementation up to a total of 250 μg/day is sufficient to prevent goiter formation during pregnancy.

Maternal Hyperthyroidism

The incidence of maternal thyrotoxicosis is about 1 per 500 pregnancies. It is accompanied by an increased incidence of prematurity, intrauterine growth restriction (IUGR), superimposed preeclampsia, stillbirth, and neonatal morbidity and mortality. Graves’ disease is an autoimmune disorder caused by thyroid-stimulating antibodies and is the most common cause of hyperthyroidism. Other causes of hyperthyroidism in pregnancy include hydatidiform mole and toxic nodular goiter. Patients with Graves’ disease tend to have a remission during pregnancy and an exacerbation during the postpartum period. The increased immunologic tolerance during pregnancy may lead to a decrease in thyroid antibodies to account for the remission.

image Heart Disease

The categories of heart disease in pregnancy include rheumatic and congenital cardiac disease as well as arrhythmias, cardiomyopathies and other forms of acquired heart disease. Better treatment of rheumatic fever and improvements in medical and surgical management of congenital heart disease has meant that in a modern tertiary referral center, about 80% of patients with cardiac disease in pregnancy now have congenital heart disease.

MANAGEMENT OF CARDIAC DISEASE DURING PREGNANCY

The New York Heart Association’s functional classification of heart disease is of value in assessing the risk for pregnancy in a patient with acquired cardiac disease and in determining the optimal management during pregnancy, labor, and delivery (Table 16-5). In general, the maternal and fetal risks for patients with class I and II disease are small, whereas risks are greatly increased with class III and IV disease or if there is cyanosis. However, the type of defect is important as well. Mitral stenosis and aortic stenosis carry a higher risk for decompensation than do regurgitant lesions. Other patients at high risk include those with significant pulmonary hypertension, a left ventricular ejection fraction less than 40%, Marfan syndrome, a mechanical valve, or a previous history of a cardiac event or arrhythmia.

TABLE 16-5 NEW YORK HEART ASSOCIATION’S FUNCTIONAL CLASSIFICATION OF HEART DISEASE

Class I No signs or symptoms of cardiac decompensation
Class II No symptoms at rest, but minor limitation of physical activity
Class III No symptoms at rest, but marked limitation of physical activity
Class IV Symptoms present at rest, discomfort increased with any kind of physical activity

Prenatal Management

As a general principle, all pregnant cardiac patients should be managed with the help of a cardiologist. A careful history and physical examination, along with an electrocardiogram and echocardiogram, should be performed. The patient should be counseled about risks associated with pregnancy and all options presented. Frequent prenatal visits are indicated, and frequent hospital admissions may be needed, especially for patients with class III and IV cardiac disease.

Avoidance of excessive weight gain and edema. Cardiac patients should be placed on a low-sodium diet (2 g/day) and encouraged to rest in the left lateral decubitus position for at least 1 hour every morning, afternoon, and evening to promote diuresis. Adequate sleep should be encouraged. If there is evidence of chronic left ventricular failure not adequately treated with sodium restriction, a loop diuretic and β blockers should be added. Aldosterone antagonists should be avoided because of their potential antiandrogen effects on the fetus.

Management of Delivery and the Immediate Postpartum Period

Cardiac patients should be delivered vaginally unless obstetric indications for cesarean are present. They should be allowed to labor in the lateral decubitus position with frequent assessment of vital signs, urine output, and pulse oximetry. Adequate pain relief is important. Pushing should be avoided during the second stage of labor because the associated increase in intraabdominal pressure increases venous return and cardiac output and can lead to cardiac decompensation. The second stage of labor can be assisted by performing an outlet forceps delivery or by the use of a vacuum extractor.

The immediate postpartum period presents special risks to the cardiac patient. After delivery of the placenta, the uterus contracts, and about 500 mL of blood is added to the effective blood volume. Cardiac output increases up to 80% above prelabor values in the first few hours after a vaginal delivery and up to 50% after cesarean delivery. To minimize the risk for overloading the circulation, careful attention is paid to fluid balance and prevention of uterine atony. Methergine should be avoided owing to its vasoconstrictor effects.

Of particular concern is the risk for endocarditis. The 2007 guidelines from the American Heart Association state that delivery does not increase the risk for infectious endocarditis. Antibiotic prophylaxis is only recommended for high-risk patients (e.g., prosthetic valves, unrepaired or incompletely repaired congenital heart disease, congenital heart disease repaired with prosthetic material, previous history of bacterial endocarditis and valvulopathy in heart transplants) if bacteremia is suspected (such as in the setting of chorioamnionitis).

Acute cardiac decompensation with congestive heart failure should be managed as a medical emergency. Medical management may include administration of morphine sulfate, supplemental oxygen, and an intravenous loop diuretic (e.g., furosemide) to reduce fluid retention and preload. β Blockers should not be used in the setting of acute heart failure. Vasodilators such as hydralazine, nitroglycerin, and rarely nitroprusside are used to improve cardiac output by decreasing afterload. Some patients may require inotropic support with dobutamine or dopamine. The use of digitalis is controversial. Angiotensin-converting enzyme inhibitors are contraindicated in pregnancy. Calcium channel blockers such as nifedipine may accelerate the progression of congestive heart failure and should be avoided. Continuous pulse oximetry can be very helpful in managing these patients. Monitoring with a pulmonary artery catheter can provide a good index of left ventricular function but is discouraged in those with pulmonary hypertension.

image Autoimmune Disease in Pregnancy

An autoimmune disease is one in which antibodies are developed against the host’s own tissues. A summary of the interactions of primary immunologic disorders and pregnancy is shown in Table 16-6.

IMMUNE (IDIOPATHIC) THROMBOCYTOPENIA

In this condition thrombocytopenia occurs when peripheral platelet destruction exceeds bone marrow production. Idiopathic thrombocytopenia (ITP) is considered to be an autoantibody disorder in which immunoglobulins attach to maternal platelets leading to platelet sequestration in the reticuloendothelial system. ITP may be confused with gestational thrombocytopenia. The latter is unlikely to have a platelet count less than 70,000/μL, is not associated with bleeding complications, occurs late in pregnancy, and resolves after delivery.

SYSTEMIC LUPUS ERYTHEMATOSUS

Lupus occurs mainly in women. Associated antibodies include antinuclear, anti-RNP and anti-SM antibodies; anti-dsDNA is associated with nephritis and lupus activity; anti-Ro (SS-A) and anti-La (SS-B) are present in Sjögren’s syndrome and neonatal lupus with heart block; while antihistone antibody is common in drug-induced lupus. The diagnosis of systemic lupus is made if 4 or more of the 11 revised criteria of the American Rheumatism Association are present, serially or simultaneously (Table 16-7).

TABLE 16-7 AMERICAN RHEUMATISM ASSOCIATION 1997 REVISED CRITERIA FOR SYSTEMIC LUPUS ERYTHEMATOSUS

Criteria Comments
Malar rash Malar erythema
Discoid rash Erythematous patches, scaling, follicular plugging
Photosensitivity  
Oral ulcers Usually painless
Arthritis Nonerosive involving two or more peripheral joints
Serositis Pleuritis or pericarditis
Renal disorder Proteinuria > 0.5 g/day or > 3+ dipstick, or cellular casts
Neurologic disorders Seizures or psychosis without other cause
Hematologic disorders Hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia
Immunologic disorders Anti-dsDNA or anti-Sm antibodies, or false-positive VDRL, immunoglobulin M or G anticardiolipin antibodies, or lupus anticoagulant
Antinuclear antibodies Abnormal titer of antinuclear antibodies

VDRL, Venereal Disease Research Laboratory.

If four criteria are present at any time during course of disease, systemic lupus can be diagnosed with 98% specificity and 97% sensitivity.

From Hochberg MC: Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 40(9):1725, 1997. Copyright 1997 American College of Rheumatology. Reprinted with permission of John Wiley & Sons, Inc.

During pregnancy, lupus improves in one third of women, remains unchanged in one third, and worsens in the remaining third. A lupus flare can be life threatening, but it is difficult to differentiate a lupus flare from superimposed preeclampsia (and both may coexist). Often only a trial of therapy will distinguish between the two. Flares and active disease can generally be managed with steroids, such as prednisone, 1 mg/kg per day.

Fetal and neonatal complications include an increased rate of preterm delivery, fetal growth restriction, and stillbirth, especially when associated with antiphospholipid antibodies. These pregnancies require close monitoring, often with weekly maternal and fetal assessments once they reach the third trimester. There is about a 10% risk for neonatal lupus, which is characterized by skin lesions, hematologic manifestations such thrombocytopenia or hemolysis, systemic effects such as hepatic involvement, and occasionally congenital heart block.

image Renal Disorders

ACUTE RENAL FAILURE

Acute renal failure during pregnancy or in the postpartum period may be due to deterioration of renal function secondary to a preexisting renal disease or to a pregnancy-induced disorder. The underlying causative factors may be prerenal, renal, or postrenal. With prerenal causes, a history of blood or fluid loss, such as occurs with obstetric hemorrhage, is usually apparent or can be elicited. Renal causes are usually suspected in a patient with a history of preexisting renal disease or with a hypercoagulable state, such as thrombotic thrombocytopenic purpura or hemolytic-uremic syndrome Prolonged hypotension can lead to acute cortical necrosis or acute tubular necrosis. Postrenal causes are less common but should be suspected in situations in which urologic obstructive lesions are present or in which there is a history of kidney stones.

Laboratory Studies

Laboratory tests are directed at assessing renal function, cardiovascular status, and the patency of the urologic tract.

Treatment

PRERENAL CAUSES

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